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甲醛通过干扰海马中硫化氢的产生损害学习和记忆。

Formaldehyde impairs learning and memory involving the disturbance of hydrogen sulfide generation in the hippocampus of rats.

机构信息

Department of Physiology, Medical College, University of South China, 28 W Changsheng Road, Hengyang, 421001 Hunan, People's Republic of China.

出版信息

J Mol Neurosci. 2013 Jan;49(1):140-9. doi: 10.1007/s12031-012-9912-4. Epub 2012 Oct 30.

Abstract

Formaldehyde (FA), a well-known indoor and outdoor pollutant, has been implicated as the responsible agent in the development of neurocognitive disorders. Hydrogen sulfide (H(2)S), the third gasotransimitter, is an endogenous neuromodulator, which facilitates the induction of hippocampal long-term potentiation, involving the functions of learning and memory. In the present study, we analyzed the effects of intracerebroventricular injection of FA on the formation of learning and memory and the generation of endogenous H(2)S in the hippocampus of rats. We found that the intracerebroventricular injection of FA in rats impairs the function of learning and memory in the Morris water maze and novel object recognition test and increases the formation of apoptosis and lipid peroxidation in the hippocampus. We also showed that FA exposure inhibits the expression of cystathionine β-synthase, the major enzyme responsible for endogenous H(2)S generation in hippocampus and decreases the production of endogenous H(2)S in hippocampus in rats. These results suggested that FA-disturbed generation of endogenous H(2)S in hippocampus leads to the oxidative stress-mediated neuron damage, ultimately impairing the function of learning and memory. Our findings imply that the disturbance of endogenous H(2)S generation in hippocampus is a potential contributing mechanism underling FA-caused learning and memory impairment.

摘要

甲醛(FA)是一种众所周知的室内和室外污染物,已被认为是导致神经认知障碍的罪魁祸首。硫化氢(H2S)是第三种气体递质,是一种内源性神经调节剂,可促进海马长时程增强的诱导,涉及学习和记忆的功能。在本研究中,我们分析了脑室注射 FA 对大鼠学习和记忆形成以及内源性 H2S 生成的影响。我们发现,脑室注射 FA 可损害大鼠在 Morris 水迷宫和新物体识别测试中的学习和记忆功能,并增加海马中细胞凋亡和脂质过氧化的形成。我们还表明,FA 暴露抑制了胱硫醚β-合酶的表达,该酶是海马中产生内源性 H2S 的主要酶,同时降低了大鼠海马中内源性 H2S 的产生。这些结果表明,FA 扰乱了海马中内源性 H2S 的产生,导致氧化应激介导的神经元损伤,最终损害学习和记忆功能。我们的研究结果表明,海马中内源性 H2S 产生的紊乱是 FA 引起学习和记忆损伤的潜在机制。

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